Emergency Medicine Syncope Case File

Emergency Medicine Syncope Case File

Eugene C. Toy, MD, Barry C. Simon, MD, Terrence H. Liu, MD, MHP, Katrin Y. Takenaka, MD, Adam J. Rosh, MD, MS

Case 15

A 64-year-old man is brought into the emergency department (ED) by his family after fainting at home. He was standing, dusting a bookshelf, when he fell backward onto the couch. He was noted to be pale and clammy during the incident, and recovered spontaneously in approximately 30 seconds. He does remember the moments just prior to and after the incident. He felt lightheaded and had palpitations just prior to falling, but does not describe any shortness of breath, chest pain, headache, nausea, diplopia, or loss of bowel or bladder control. His history includes a myocardial infarction 2 years prior. The patient has been taking his regular medicines as directed, which include aspirin, a β-blocker, and a cholesterol- lowering agent. His primary medical doctor has not recently started any new medicines or changed his doses. On presentation to the ED, the patient’s vitals are blood pressure 143/93 mm Hg, heart rate of 75 beats per minute, respiratory rate of 18 breaths per minute, temperature of 37.1°C (98.8°F), and oxygen saturation of 97% on room air. His examination is significant for a cardiac gallop. No carotid bruits, neurological abnormalities, rectal bleeding, or orthostatic changes are noted. A 12-lead electrocardiogram (ECG) demonstrates a normal sinus rhythm at 75 beats per minute with no significant changes from a prior study 6 months earlier; the ECG reveals Q waves in leads II, III, and aVF. The patient now states he feels fine and would like to go home.

⯈ What is the most likely diagnosis?

⯈ What is your next step?

ANSWER TO CASE 15:

Syncope

Summary: This is a 64-year-old man with a medical history that includes a myocardial infarction who presents with an episode of syncope. The patient has an ECG with inferior Q waves, but no acute changes at the time of presentation.

• Most likely diagnosis: Syncope, most likely caused by a cardiac dysrhythmia with spontaneous resolution
• Next step: Management of ABCs, intravenous access, and initiation of continuous cardiac monitoring

ANALYSIS

Objectives

1. Recognize worrisome historical and physical features of syncope.
2. Understand the emergency physician’s (EP’s) role in evaluation of patients with syncope, and the role of selective diagnostic testing.
3. Learn to recognize which patients need to be admitted to the hospital.

Considerations

Syncope has many etiologies that are often difficult to identify with certainty in the ED. The goal of the EP is to identify and treat any life threats. If there is no critical immediate treatment needed, the goal is then to risk stratify patients for the likelihood of an adverse outcome. The patient in this case is at high risk for a cardiac etiology of his syncope. This patient should be immediately placed on a cardiac monitor and receive an intravenous line. The physician should treat any abnormal findings. If the patient appears dehydrated, he should receive intravenous fluids. If a dysrhythmia exists (eg, ventricular tachycardia), it should be immediately addressed with either cardioversion or defibrillation. If the patient appears stable, the workup should proceed with the patient maintained on the cardiac monitor. The decision to admit or discharge the patient depends on many factors. However, if there is suspicion that there is a cardiac etiology for syncope, this patient should be admitted to a monitored hospital bed.

Approach To:

Syncope

DEFINITIONS

SYNCOPE: A transient loss of consciousness with a corresponding loss of postural tone, with a spontaneous and full recovery.

PRESYNCOPE: A sensation that one is about to lose consciousness, usually with nonspecific symptoms consistent with a prodrome of syncope such as lightheadedness, weakness, dizziness, blurred vision, or nausea.

VASOVAGAL SYNCOPE: A form of neurocardiogenic syncope, which occurs in the setting of increased peripheral sympathetic activity and venous pooling.

CLINICAL APPROACH

Syncope is an extremely common presenting symptom to the ED, accounting for approximately 5% of all ED visits in this country. Between 1% and 6% of hospitalized patients are admitted for an evaluation of syncope. The list of potential etiologies of syncope is extensive; causes include cardiac, reflex-mediated, orthostatic (eg, postural hypotension caused by volume depletion, sepsis-related peripheral vasodilation, or medications), psychiatric, hormonal, neurologic, and idiopathic. Unnecessary or inappropriate ancillary testing can consume thousands of dollars per patient and increase ED length of stay. With a carefully taken history and physical examination, clinicians can better risk stratify patients and determine who needs to be admitted to the hospital for further evaluation and who can be safely discharged for outpatient workup.

Etiologies

Cardiac syncope refers to the loss of postural tone secondary to a sudden and dramatic fall in cardiac output. Bradydysrhythmias, tachydysrhythmias, heart block, and mechanisms that disrupt outflow or preload are the functional physiologic abnormalities that cause these sudden changes in blood flow and ultimately inadequate perfusion of the brain. Patients with various forms of organic heart disease (eg, aortic stenosis and hypertrophic cardiomyopathy), and those with coronary artery disease, congestive heart failure, ventricular hypertrophy, and myocarditis are at highest risk. Causes of bradydysrhythmias include sinus node disease, second/ third-degree heart block, and pacemaker malfunction. Tachydysrhythmias include ventricular tachycardia, ventricular fibrillation, torsades de pointes, and supraventricular tachycardia of both nodal and atrial origin, some of which may be associated with conditions such as Wolfe-Parkinson-White syndrome, Brugada syndrome, or long QT syndrome. When syncope is precipitated by a tachydysrhythmia, patients may complain of palpitations. Mechanical etiologies such as pericardial tamponade and aortic dissection should be considered in causes of cardiac syncope as both entities will result in a significant fall in functional cardiac output. Massive pulmonary embolism must also be considered, as it can lead to syncope caused by right ventricular outflow obstruction which, in turn, leads to a fall in left-sided filling pressure. Right-sided ventricular strain and dilatation can also lead to dysrhythmia.

Reflex-mediated syncope, also known as situational syncope, includes vasovagal, cough, micturition, defecation, emesis, swallow, Valsalva, and emotionally (eg, fear, surprise, disgust) related syncope. Loss of consciousness and motor tone is caused by stimulation of the vagal reflex, resulting in transient bradycardia and hypotension. Warmth, nausea, lightheadedness, and the impending sense that often precedes loss of consciousness are common complaints of those affected by vagal syncope.

Carotid sinus disease or stimulation of overly sensitive baroreceptors in the neck (a tight collar) are other causes of sudden reflex-related syncope. These patients will often note a specific activity that is temporally related to their syncopal episodes (turning the head in a certain direction). A recent examination of the Framingham cohort found that patients who were clearly identified to have syncope of vasovagal etiology were not at any increased risk of cardiovascular morbidity or mortality. Unfortunately, making a firm diagnosis of vasovagal syncope in the setting of the ED is difficult, and it should be a diagnosis of exclusion.

Orthostasis (ie, a drop in systolic blood pressure of 20 mm Hg or more resulting from a rapid change in body position from a supine to more upright posture) is another common cause of syncope. Diaphoresis, lightheadedness, and graying of vision may suggest orthostatic syncope, and recurrence of these symptoms on standing is more significant than the actual numeric change in blood pressure. However, orthostasis may be present in up to 40% of patients older than the age of 70 who are asymptomatic. Orthostatic hypotension can be related to volume depletion, sepsisrelated peripheral vascular dilation, medications, and autonomic instability, which can develop in a number of chronic illnesses such as diabetes, Parkinson disease, multiple sclerosis, and other neuromuscular disorders. Volume depletion secondary to sudden blood loss needs to be considered in all patients with syncope. Patients of all ages can develop a sudden gastrointestinal (GI) bleed and the initial blood flow can be occult because it is confined to the lower GI tract. Elderly patients can lose massive amounts of blood from a leaking or ruptured abdominal aortic aneurysm, with abdominal or flank pain as common associated complaints, but syncope alone can also be the presenting complaint. In the female patient of childbearing age, normal intrauterine or ruptured ectopic pregnancy may present with syncope. The former may cause orthostasis as a result of the normal cardiovascular changes associated with pregnancy, and the latter as the only manifestation of life-threatening hemorrhage.

Hypotension leading to syncope is not necessarily related to volume loss. Patients, particularly the elderly, may present with syncope as the first overt manifestation of sepsis. Hypotension in these patients is caused by relative lack of intravascular volume secondary to decreased vascular tone as part of the inflammatory response. Patients with a history of hypertension may have what appears to be a “normal” blood pressure when they are actually in a state of relative hypotension.

Medication, especially polypharmacy, a common problem in the elderly, is another important cause of syncope. Antihypertensives, antidepressants, antianginals, analgesics, central nervous system depressants, medications that can prolong the QT interval (eg, erythromycin, clarithromycin, haloperidol, amiodarone, droperidol, and others), insulin, oral hypoglycemics, and recreational polypharmacy are common culprits. Geriatric patients with complicated medical histories are particularly at risk, although a detailed ingestion history should be obtained from all patients presenting with syncope. One should look closely for recent additions or changes to a medication regimen, including over-the-counter medications.

Neurologic causes of syncope are rare, unless seizure is included in the differential diagnosis; seizure and syncope should be differentiated and thought of as discrete diagnoses. Seizure can usually be quickly identified by the history of witnessed seizure activity, especially if accompanied by a history of seizures in the past. It is also suggested by physical examination findings (eg, tongue biting, loss of bowel/bladder control) and especially the observation of a postictal state, which commonly resolves over a period from several minutes to many hours. Brief tonicclonic activity, resulting not from a seizure focus, but from the transient hypoxia of the brain stem, which leads to loss of consciousness, may be associated with syncope. However, the duration of confusion or lethargy following the episode is short lived. The sudden onset of a severe headache associated with loss of consciousness suggests a subarachnoid hemorrhage as the cause of syncope. Other neurological causes of syncope include migraines, subclavian steal, and transient ischemic attack or stroke of the vertebrobasilar distribution.

Sometimes patients with psychiatric disease will present with the complaint of sudden loss of consciousness. The history of these patients may include several prior episodes of syncope. Typically, these incidents will present with minimal physical trauma and none of the signs or symptoms that are commonly associated with cardiac syncope. Anxiety, with or without hyperventilation, conversion disorder, somatization, panic attacks, and breath-holding spells are all manifestations of psychiatric illness that can cause syncope. However, psychiatric and emotional etiologies of syncope are considered a diagnosis of exclusion. This diagnosis should be considered only after appropriate laboratory or ancillary testing has ruled out more serious etiologies. Furthermore, it must be recognized that many of the most commonly prescribed neuroleptics cause QT prolongation, which in turn, can lead to ventricular dysrhythmia.

Diagnosis

Much to the frustration of patients and providers, the underlying cause of the syncopal presentation is not elucidated in approximately half of patients who present to the ED with syncope. Unfortunately, patients in this category represent a mixed population in which it is estimated that anywhere between 45% and 80% may have had a cardiac cause. Most of the young and otherwise healthy patients will be discharged home without a clearly defined cause for their loss of consciousness. Many of the elderly patients will be admitted for additional testing and observation. Of all the diagnostic tools available to physicians in the evaluation of syncope, a good thorough history, a physical examination, and ECG are the only level A recommendations from the American College of Emergency Physicians (ACEP). The information gathered from the history and physical examination alone will identify the potential cause of syncope in 45% of cases.

The goal of the initial evaluation is to find out exactly what happened to the patient. It is critical to ascertain a step-by-step history of the event. This includes getting a detailed account from any bystanders or family members, which can be valuable in making the correct diagnosis. The history and complete physical examination, combined with the electrocardiogram, form the preliminary workup of patients with syncope. Orthostatic blood pressure measurements should be obtained if orthostasis is likely.

This approach is often suggestive of a diagnosis in cases of vasovagal, situational, orthostatic, polypharmacy, and some cardiac-related syncope. Although vasovagal and situational syncope may be strongly suspected based upon the history, a true diagnosis of vasovagal syncope requires additional testing not available in the ED. While vasovagal/situational syncope does occur in elderly patients, it is a diagnosis that cannot be safely relied upon in the ED unless the history is completely indicative (ie, syncope at the sight of blood) and there are no physical or diagnostic test findings that raise concern for more ominous causes. Elderly patients are also at risk for serious injuries such as hip fractures from even relatively benign causes of syncope. Although older patients admitted with a story consistent with vasovagal syncope may ultimately leave the hospital with that diagnosis, the risk profile of elderly patients as a whole almost always makes this a diagnosis that cannot be determined within the confines of the ED. However, young, healthy patients with histories consistent with vasovagal syncope may be approached with less diagnostic testing. Younger patients should be questioned regarding a family history of early cardiac or sudden death; although rare, certain genetic conditions such as Brugada syndrome, hypertrophic cardiomyopathy, and long QT syndrome may present with syncope.

Laboratory Tests

Although laboratory testing rarely elucidates the cause of the syncope, it can be helpful in a limited number of situations. Inexpensive laboratory tests include complete blood count (CBC) for blood loss, glucometer for hypoglycemia, and electrolytes and blood urea nitrogen/creatinine levels for dehydration. Toxicology screening for drug-related syncope is rarely helpful for the immediate evaluation and stabilization of the patient. Furthermore, assumption of a toxicologic cause should not deter the physician from performing a complete evaluation. A urinalysis is an inexpensive and useful screening test that can provide information about glucose, infection, the patient’s state of hydration, and the presence or absence of ketones. A urine pregnancy test should always be obtained in women of childbearing age, because early pregnancy and ectopic pregnancy can present as syncope.

Management

Patients with history or examination findings suggestive of a particular pathology should undergo continuous cardiac monitoring, echocardiography, Doppler vascular studies, or contrast computed tomography (CT) imaging. Those patients with unexplained syncope and high-risk clinical features (eg, advanced age, abnormal electrocardiogram, previous cardiac history, exertional syncope) require admission for further investigation such as tread-mill testing, tilt-table testing, CT imaging of the head, cardiac enzymes, cardiac catheterization, and electrophysiologic studies.

While diagnosis and treatment are the goals in the evaluation of syncope, the decision tree for EM physicians is more focused than that of the specialist or outpatient physician (Figure 15–1). Unstable patients presenting after a syncopal episode, including those with persistent hypotension, life-threatening dysrhythmias, active blood loss, acute coronary syndromes, hemodynamically significant pulmonary emboli, and cardiac tamponade must be managed emergently. The “ABC” (airway, breathing, circulation) approach to the unstable patient applies in this scenario as in all presentations with unstable vital signs. History and physical examination in

Figure 15–1. Algorithm of syncope evaluation.

the context of syncope should guide diagnostic thinking, but should not substitute for emergent management considerations.

Disposition

For the patient who presents after syncope but is hemodynamically normal at the time of presentation, the decision to admit versus discharge from the ED with outpatient follow-up is dependent on other clinical features suggesting that the patient is at high risk for a short-term adverse outcome.

Several studies have tried to aid the EM physician in identifying high-risk patients by using clinical decision rules (Table 15–1). The San Francisco Syncope Rule, the OESIL (Osservatorio Epidemiologico sulla Sincope nel Lazio), and the ROSE (Risk Stratification of Syncope in the Emergency Department) are decision rules that attempt to provide clinicians with patient characteristics associated with an increased likelihood for an adverse outcome The San Francisco Syncope rule uses five criteria: history of CHF, abnormal ECG, hematocrit <30, shortness of breath, and/or systolic BP of <90 mm Hg at triage, to predict who requires hospitalization. The OESIL score is based upon abnormal ECG, history of cardiac disease, age >65, and syncope without prodrome. The ROSE predictors are: BNP >300, positive fecal

Abbreviations: OESIL = Osservatorio Epidemiologico sulla Sincope nel Lazio; ROSE = Risk stratifi cation of syncope in

the emergency department.

Based on data from SFSR: San Francisco Syncope Rules.

occult blood, hemoglobin <9.0, oxygen saturation <94%, and Q waves present on ECG. The Rose rule is the first to incorporate a biochemical marker, BNP, into the criteria and claims a sensitivity and negative predictive value of 87.2% and 98.5%, respectively. An abnormal ECG is the only common thread in all three rule sets (Figure 15–2), although “abnormal” may be defined in a variety of ways. If the biochemical marker BNP in the ROSE criteria is considered a surrogate for a history of CHF, this reinforces that known cardiac disease is a factor associated with high-risk patients. Regardless of which rule set one considers, it should be recognized that decision tools and algorithms should never be used as a substitute for a full evaluation and individualized clinical judgment of all aspects of the patient’s presentation. Many of these decision rules are still undergoing evaluation in an effort to gain validation. In fact, a recent analysis comparing the efficacy of risk stratification using the San Francisco and OESIL rule sets versus clinical judgment on short-term prognosis found that both rule sets had relatively low sensitivities. Having to use both rule sets would be needed to identify all patients who subsequently died, and the best results were obtained if a clinician used a combination of clinical knowledge with a rule set.

The American College of Emergency Physicians (ACEP) clinical policy guidelines emphasizes risk stratification of patients presenting with syncope in a similar fashion to those presenting with chest pain. It is generally accepted that historical or physical examination findings consistent with heart failure, structural or coronary heart disease, as well as an abnormal ECG are linked with high risk of poor outcome. Advancing age is coupled with a continuum of growing cardiovascular risk and should also be a consideration. It also bears mentioning that in the highrisk groups, however they are defined, presyncopal events should be evaluated and managed as syncope, because the etiologies are the same and are distinguished only by the degree of hypoperfusion of the brain. The younger patient with no comorbidities, reassuring first-time symptoms, and a normal electrocardiogram can usually be discharged from the ED. Referral to a primary medical doctor should be made for coordination of any outpatient studies that may be warranted in the evaluation of recurring syncope. Patients with specific job-related concerns, such as heavy machine operators, pilots, or physicians, may require more expeditious referral and notification of the appropriate State authorities. Even benign causes of syncope, such as vasovagal syncope, can be fatal when the patient is driving.

Predictor Variables of Risk Rules

SFSR: San Francisco Syncope Rules

OESIL: Osservatorio Epidemiologico sulla Sincope nel Lazio

ROSE: Risk Stratification of Syncope in the Emergency Department

Figure 15–2. Predictor variables of risk rules.

COMPREHENSION QUESTIONS

15.1 A 37-year-old man is brought into the ED because he passed out at work. He denies any prodromal symptoms. Family history is negative for sudden cardiac death. In the ED, his BP lying down is 125/75 mm Hg, heart rate is 75 beats per minute, and respiratory rate is 14 breaths per minute. The patient’s blood pressure and heart rate standing are 120/75 mm Hg and 77 beats per minute, respectively. His ECG shows a sinus rhythm with a rate of 72. Physical examination does not reveal any abnormal findings. Currently, he is lucid and has no neurologic abnormalities. After a complete evaluation of this patient, which of the following is the most common etiology of syncope?

A. Dysrhythmia

B. Orthostasis

C. Idiopathic

D. Situational

15.2 A 35-year-old woman presents to the ED complaining of feeling lightheadedness. She noticed some vaginal bleeding earlier in the day. Her blood pressure is 85/53 mm Hg, heart rate is 130 beats per minute, and respiratory rate is 18 breaths per minute. Which of the following is the most appropriate next step in management?

A. Obtain a urine pregnancy test.

B. Obtain a serum quantitative beta human chorionic gonadotropin (β-hCG).

C. Obtain immediate IV access and begin fluid resuscitation.

D. Obtain stat OB/GYN consult.

15.3 A 21-year-old man is brought to the ED after collapsing to the ground while playing basketball. He is alert and oriented, denies chest pain, difficulty breathing, or any other physical complaints. There was no trauma. He denies any past medical problems. Physical examination is unremarkable. Which of the following elements on his ECG is concerning for a life-threatening cause of syncope?

A. Heart rate of 55

B. P-wave inversion in lead aVR

C. Sinus arrhythmia

D. QTc of 495 msec

15.4 A 72-year-old man is brought to the ED by paramedics after passing out at the supermarket. His syncopal episode was witnessed by shoppers who stated the patient collapsed, hitting his head. The patient is currently alert and oriented, and denies any persistent symptoms. His past medical history is significant for carotid stenosis, for which he takes aspirin and clopidogrel. What is most appropriate next step in the management of this patient?

A. Head CT scan

B. Order a carotid duplex ultrasound

C. Obtain an ECG

D. Chest radiograph

ANSWERS

15.1 C. Idiopathic. Approximately 50% of all patients with a presenting complaint of syncope will not have a definitive cause. Cardiac causes of syncope (eg, dysrhythmia) are the most worrisome, because patients are at increased risk for sudden cardiac death. Situational syncope is a rare cause of syncope. It is a result of an abnormal autonomic reflex response to a physical stimulus. Some triggers of this response include coughing, swallowing, defecation, and micturition. The patient does not have evidence for orthostatic hypotension as demonstrated by his vital signs.

15.2 C. Obtain IV access and begin fluid resuscitation. Investigating the possibility of pregnancy, specifically ectopic pregnancy, is critical. However, initial stabilization of the patient takes precedence. Hypotension must be treated emergently with fluids. Obtaining a consult early in the patient’s course is important. Definitive management will be in the operating room.

15.3 D. The upper level of normal for the corrected QT interval is approximately 440 msec for men and 460 msec for women. A finding of a prolonged QT interval should prompt a more thorough investigation into this patient’s medications, family history, and potential electrolyte imbalances. Prolonged QT syndrome is associated with sudden death, especially in young athletes. Mild bradycardia alone in a young, healthy patient who has fully recovered from an episode of syncope is of little concern. P-wave inversion in lead aVR is a normal finding. Sinus arrhythmia is a normal variation in the RR interval with respiration.

15.4 C. Obtain an ECG. This patient has a high probability for a cardiac cause of his syncope. Initial management includes placing the patient on a cardiac monitor and obtaining an ECG to monitor for dysrhythmias. A head CT scan should be performed after an ECG is obtained. A carotid duplex ultrasound and chest radiograph may aid in the workup for syncope, but it is most important to first rule out a dysrhythmia.

CLINICAL PEARLS

⯈ The primary goal of the EP in the evaluation of patients with syncope is to be able to identify those who are at high risk for morbidity and mortality.

⯈ The causes of syncope are varied, and a successful diagnosis hinges on diligent history collection and appropriate use of diagnostic tools.

⯈ Even the most experienced clinician will be unable to determine the cause of syncope in up to 50% of patients.

⯈ Reassuring clinical signs in syncope are youth, a normal ECG, absence of comorbidities, and reassuring historical features.

⯈ Unstable patients should be treated emergently and stabilized, first addressing the ABCs.

References

American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of patients presenting with syncope. Ann Emerge Med. 2007;49:431-444. 

Carlson, MD. Syncope. In: Harrison’s Principles of Internal Medicine. 17th ed. New York, NY: McGraw-Hill; 2008. 

Colivicchi F, Ammirati F, Melina D, et al. Development and prospective validation of a risk stratification system for patients with syncope in the emergency department: the OESIL risk score. Eur Heart J. 2003;24:811. 

De Lorenzo RA. Syncope. In: Rosen’s Emergency Medicine: Concepts and Clinical Practice. 6th ed. St Louis, MO: Mosby; 2005. 

Dipaola FCG, Perego F, Borella M, et al. San Francisco Syncope Rule, Osservatorio Epidemiologico sulla Sincope nel Lazio risk score, and clinical judgment in the assessment of short-term outcome of syncope. Am J Emerg Med. 2010;28:432-439. 

Dovgalyuk J, Holstege C, Mattu A, Brady WJ. The electrocardiogram in the patient with syncope. Am J Emerg Med. 2007;25(6):688-701. 

Huff JS, Decker WW, Quinn JV, et al; American College of Emergency Physicians. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the ED with syncope. Ann Emerg Med. 2007;49:431-434. 

Kessler C, Tristano JM, DeLorenzo R. The emergency department approach to syncope: evidence-based guidelines and prediction rules, Emerg Med Clin N Am. 2010; 28:487-500. 

Linzer M, Yang EH, Estes NA, et al. Diagnosing syncope part 1: value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996. 

Linzer M, Yang EH, Estes NA, et al. Diagnosing syncope part 2: unexplained syncope. Ann Intern Med. 1997;127(1):76-84. 

Quinn, J. Syncope. In: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. McGraw-Hill; 2011. 

Quinn JV, Stiell IG, McDermott DA, et al. Derivation of the San Francisco syncope rule to predict patients with short-term serious outcomes. Ann Emerg Med. 2004;43:224-232. 

Reed MJ, Newby DE, Coull AJ, et al. The ROSE (Risk Stratification of Syncope in the Emergency Department) Study. J Am Coll Cardiol. 2010;55 (8):713-721. 

Schipper JL, WN Kapoor. Cardiac arrhythmias: diagnostic evaluation and management of patients with syncope. Med Clin North Am. 2001;85(2):423-456. 

Serrano LA, Hess EP, Bellolio MF, et al. Accuracy and quality of clinical decision rules for syncope in the emergency department: a systematic review and meta-analysis. Ann Emerg Med. 2010;56(4):362-373. 

Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. New Engl J Med. 2002;347:878-885. 

Sun BC, Emond JA, Camargo CA Jr. Direct medical costs of syncope-related hospitalizations in the United States. Am J Cardiol. 2005;95(5):668-671.

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